Excitation energy transfer and charge separation are affected in Arabidopsis thaliana mutants lacking light-harvesting chlorophyll a/b binding protein Lhcb3

The composition of LHCII trimers as well as excitation energy transfer and charge separation in grana cores of Arabidopsis thaliana mutant lacking chlorophyll a/b binding protein Lhcb3 have been investigated and compared to those in wild-type plants. In grana cores of lhcb3 plants we observed increased amounts of Lhcb1 and Lhcb2 apoproteins per PSII core. The additional copies of Lhcb1 and Lhcb2 are expected to substitute for Lhcb3 in LHCII trimers M as well as in the LHCII "extra" pool, which was found to be modestly enlarged as a result of the absence of Lhcb3. Time-resolved fluorescence measurements reveal a deceleration of the fast phase of excitation dynamics in grana cores of the mutant by ∼ 15 ps, whereas the average fluorescence lifetime is not significantly altered. Monte Carlo modeling predicts a slowing down of the mean hopping time and an increased stabilization of the primary charge separation in the mutant. Thus our data imply that absence of apoprotein Lhcb3 results in detectable differences in excitation energy transfer and charge separation

Monte Carlo simulations of excitation and electron transfer in grana membranes

AbstractTime-resolved fluorescence measurements on grana membranes with instrumental response function of 3ps reveal faster excitation dynamics (120ps) than those reported previously. A possible reason for the faster decay may be a relatively low amount of “extra” LHCII trimers per reaction center of Photosystem II. Monte Carlo modeling of excitation dynamics in C2S2M2 form of PSII–LHCII supercomplexes has been performed using a coarse grained model of this complex, constituting a large majority of proteins in grana membranes. The main factor responsible for the fast fluorescence decay reported in this work was the deep trap constituted by the primary charge separated state in the reaction center (950–1090cm−1). This value is critical for a good fit, whereas typical hopping times between antenna polypeptides (from ~4.5 to ~10.5ps) and reversible primary charge separation times (from ~4 to ~1.5ps, respectively) are less critical. Consequently, respective mean migration times of excitation from anywhere in the PSII–LHCII supercomplexes to reaction center range from ~30 to ~80ps. Thus 1/4–2/3 of the ~120-ps average excitation lifetime is necessary for the diffusion of excitation to reaction center, whereas the remaining time is due to the bottle-neck effect of the trap. Removal of 27% of the Lhcb6 apoprotein pool by mutagenesis of DEG5 gene caused the acceleration of the excitation decay from ~120 to ~100ps. This effect may be due to the detachment of LHCII-M trimers from PSII–LHCII supercomplexes, accompanied by deepening of the reaction center trap